We and others have shown that Lys-bradykinin (BK) is rapidly generated during airway inflammation. We hypothesize that the kinin system is organized to respond initially through the B2 BK receptor expression based on recent observations made in Dr. Zuraw's laboratory. The B1 BK receptor is then postulated to play an important role in sustaining and amplifying chronic inflammation. Our goal is to analyze the regulation of B1 BK receptor expression and functional consequences of its activation employing an experimental human model of chronic allergic inflammation. Our specific aims are to 1) assess the effects of in vivo allergic inflammation on B1 BK receptor expression in the airway; 2) characterize the effect of experimental challenge with B1 BK receptor agonist Lys-[des-Arg9]-BK on inflammatory gene expression in the airway. The studies in this proposal will provide some of the first information about the potential role of the B1 BK receptor in human inflammation. By analyzing B1 BK receptor upregulation following allergen provocation as well as the link between B1 BK receptor agonist stimulation and transcription factor activation, we will provide a framework for understanding the role of B1 BK receptor in allergic airway inflammation.